Hyperplasia of pancreatic beta cells and improved glucose tolerance in mice deficient in the FXYD2 subunit of Na,K-ATPase

Abstract

Background: Reduction in functional beta cells in pancreas is the major obstacle in diabetes. Results: Mice deficient in FXYD2 subunit of Na,K-ATPase possess a metabolic phenotype of low blood glucose along with hyperplastic pancreatic islets and hyperinsulinemia. Conclusion: The phenotype observed in Fxyd2-/- mice results from an increase in beta cell mass. Significance: FXYD2 may be a novel target for development of cell-based interventions in diabetes. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.